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University of the East Ramon Magsaysay Memorial Medical Center Department of Clinical Neurosciences College of Medicine III – Medicine Interviewer: Jorge Gabriel Ang S> Patient is a 67 year old male admitted with a complaint of sudden weakness of the left side extremities and slurring of speech of a few minutes duration right after waking up. He was immediately brought to the UERM for consult and admission. Patient is a diagnosed diabetic of 20 years, taking Glipizide and Metformin with good compliance. He also had a history of a previous stroke. He was also a smoker of unrecalled pack years who had stopped. O> Physical examination shows blood pressure of 130/80 mmHg and harsh breath sounds on auscultation. Cranial nerve exam shows preferential gaze drift to the right with difficulty reaching midline and left central facial palsy. Motor examination shows loss of muscle strength on the left upper and lower limbs with a positive Babinski reflex on the left. A> Problem I: Left Central Facial Palsy and Right Preferential Gaze The facial nerve is the nerve that innervates the muscles of expression of the face; a facial palsy refers to the loss of innervation of the facial muscles resulting in loss of muscle activity and tone, observed when the patient is unable to make facial expressions such as smiling and frowning. Central facial palsy is a specific palsy indicating loss of innervation of the lower half of the paretic side, in this case indicating that the lesion is an upper motor neuron lesion because the upper aspect of the face is innervated by the facial nerve bilaterally whereas the lower face is only innervated by the contralateral nerve. A lower motor neuron lesion would cut off the nerve entirely, causing the entire side of the face to become paretic rather than a specific quadrant, hence differentiating it from an UMN lesion. Preferential gazes, meaning that the eyes drifts towards a specific side rather than at midline, occurs when the motor nerves innervating the extra-ocular muscles of one eye are lost or reduced, causing a relative imbalance of the strength of the muscles between both eyes, thus the drift towards the side where the innervation is stronger. In a right preferential gaze, the eyes drift towards the right, suggesting that there is a loss of innervation of the muscles on the left eye, specifically the left lateral rectus innervated by the abducens nerve which pulls the eye laterally. These two conditions together suggest an upper motor neuron lesion affecting the facial section of the motor homunculus. Problem II: Left Sided weakness with Babinski Sign Loss of muscle strength and a positive Babinski sign is indicative of an upper motor neuron lesion affecting the motor homunculus governing the limbs. The Babinski sign, which is the fanning of the toes on the affected side when the lateral plantar aspect is stimulated, occurs due to the absence of an upper motor neuron’s inhibitory control over the primitive reflexes of the lower motor neurons. Hence a Babinski sign is an effective tool in localizing a lesion. Primary Diagnosis: Left Middle Cerebral Artery Embolic Infarction The left middle cerebral artery is considered the main artery feeding the motor homunculus on the left cerebral hemisphere, supplying the majority of the primary motor cortex as well as the frontal and parietal lobes. Loss of blood supply to the middle cerebral artery causes varying degrees of effects depending on the location of the lesion. The most common causes of tissue infarction from a MCA lesion is due to a thromboembolic infarction, a developed atherosclerotic plaque or a ruptured bleeding aneurysm. Given that the patient has a previous history of a stroke and has risk factors for the development of atherosclerosis such as his advanced age, previous smoking history and his type 2 diabetes mellitus, it is most likely that the patient suffered a thromboembolic infarction that blocked the MCA segment feeding the primary motor cortex that has manifested as loss of motor function over the left side of the body and face with a positive Babinski sign. A thromboembolic infarction that was likely thrown off from a remote site is the likely cause due to the sudden onset of the patient’s signs and symptoms, as opposed to a plaque or an aneurysm, which occurs gradually or stepwise, respectively. P> Diagnostic Workup I. Cranial CT Scan Cranial vault imaging is now the modality of choice for locating infracted sites along the central nervous system proper, showing radioopacity changes on the site of infarction revealing cellular degeneration of the neurons, specifically on the motor cortex along the postcentral gyrus of the parietal lobe. A CT scan will be able to localize the location of the bleed and help confirm the diagnosis. Treatment Plan I. Tissue Plasminogen activator In the ER setting, the drug of choice for thrombolysis in the event of a CVA is tPA, a protein that activates plasmin and the body’s natural thrombolytic mechanism to dissolve intravascular blood clots, and in the case of CVA dissolve the formed thrombus over the MCA, and is considered effective when given within 3 hours of onset of symptoms. The preferred dose is 0.9mg/kg. II. Anti-platelet Medication COX-2 inhibitors, which inhibit the functions of platelets, are used as long term medication for the prevention of future thromboembolic events by reducing the possibility of the formation intravascular blood clots which can become the source of future embolic events. Anti-platelet medications with drugs such as aspirin are considered beneficial in preventing future vascular events.